Elevation of glutathione levels and glutathione S-transferase activity in arsenic-resistant chinese hamster ovary cells |
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Authors: | T C Lee M L Wei W J Chang I C Ho J F Lo K Y Jan H Huang |
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Institution: | (1) Institute of Biomedical Sciences, Academia Sinica, 11529 Taipei, Taiwan (R.O.C.);(2) Institute of Zoology, Academia Sinica, 11529 Taipei, Taiwan (R.O.C.);(3) Institute of Radiation Biology, National Tsing-Hua University, 30043 Hsinchu, Taiwan (R.O.C.) |
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Abstract: | Summary Arsenic-resistant Chinese hamster ovary (CHO) cells were established by progressively increasing the concentration of sodium
arsenite in culture medium. One of the resistant clones, SA7, was also cross-resistant to As(V), Zn, Fe(II), Co, and Hg. The
susceptibilities to sodium arsenite in parental CHO cells, revertant SA7N cells, and resistant SA7 cells were correlated with
their intracellular glutathione (GSH) levels and glutathione S-transferase (GST) activity. The resistance in SA7 cells was
diminished by depletion of GSH in cells after treatment with buthionine sulfoximine. Furthermore, after reexposure of revertant
SA7N cells to sodium arsenite, the intracellular GSH levels, GST activity, and resistance to sodium arsenite were raised to
the same levels as SA7 cells. These data indicate that the elevation of intracellular GSH levels and GST activity in SA7 cells
may be responsible for the resistance to arsenite. A p25 protein, which could be a monomer subunit of GST, accumulated in
SA7 cells. In addition, an outward transport inhibitor, verapamil, indiscriminately increased the arsenite toxicity in resistant
and parental cells.
This work was supported in part by grant NSC77-0201-B001-31 from the National Science Council, Republic of China. |
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Keywords: | arsenic-resistance glutathione glutathione S-transferase |
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